Field of the Invention
The present invention relates to plants having increased resistance to pests through alteration of plant susceptibility genes and methods of producing the same.
Description of Related Art
Many parasitic insects and microbes attack plants by suppressing plant defenses and inducing other changes to the benefit of the pest. Often, the manipulation of plants by parasites is a necessary prerequisite for host susceptibility. Mayetiola destructor (MD, the Hessian fly), a destructive insect pest of wheat, is one example of these types of parasitic insects. The Hessian fly is a gall midge, and galling insects, such as the Hessian fly, manipulate host plants to induce the formation of galls (nutritive cells) for the benefit of the insect, as well as alter plant metabolism. The Hessian fly, in particular, manipulates host plants extensively. A single Hessian fly larva (less than 1 μm long) can irreversibly inhibit wheat growth, induce the formation of nutritive tissue at the feeding site, and reprogram metabolic pathways of susceptible host plants. As a result, an infested plant becomes stunted, and the whole plant acts like a gall with the insect feeding site as the nutrient sink. If plant manipulation and thus the formation of galls is prevented, galling insects cannot survive and plants become resistant to attack. Previously, the Hessian fly and other parasitic pests have been controlled by developing cultivars with resistance mediated by major resistance (R) genes that have a typical gene-for-gene interaction with pest avirulence. According to the general gene-for-gene theory of resistance, a successful resistance is triggered only if a resistance gene product in the plant recognizes a specific avirulence gene product from the pest. This effector-triggered immunity in plants is widely employed as a cost-effective and environmentally-friendly measure for pest management. The major challenge for this resistance gene approach is that the period of effective resistance mediated by R genes is short, lasting only about 6-8 years. This short-lived resistance is a major hindrance for wide adaptation of cultivars with resistance to multiple pests.
In addition, compatible and incompatible interactions can be temperature sensitive. That is, susceptibility can reoccur, even in plants containing R genes, if the plants are shifted to a temperature exceeding their normal growth temperature by a certain number of degrees. For wheat, this temperature is approximately 10° C. higher than their normal growth temperature of about 20° C. Thus, the effect of the R genes can be neutralized by high temperature, which suggests a relationship between plant resistance and susceptibility as follows. In particular, one or more targets exist in the plant essential for susceptibility manipulation by the pest. When these targets are activated, through either increased expression or other means during compatible interactions, plants can be successfully manipulated by the pest and become susceptible. When the activation of these targets is prevented through an R gene effect, plants cannot be manipulated by the pest and therefore are resistant. The targets can also be activated in plants under high temperature independent of the R gene effect, and the activation of the targets is sufficient for the pests to manipulate plants, resulting in plant susceptibility even in the presence of an R gene. Most, if not all, Hessian fly resistance genes identified in wheat are temperature sensitive, and resistance is lost when the plants are exposed to high temperature (30-37° C.) for a given period of time.
Thus, there remains a need in the art for improved methods of increasing plant resistance to pests, even under elevated temperature conditions.